Enterococcal bacteremia in a medical center

BACKGROUND: The enterococci have become important nosocomial pathogens. They can cause multiple site infections and enterococcal bacteremia becomes more frequently associated with a high mortality rate. Previous studies of enterococcal bacteremia showed a variety of results. To establish the significance and importance of enterococci as nosocomial pathogens in this hospital, to characterize their clinical pictures and to search for the risk factors for mortality, this retrospective study was performed. METHODS: There were 208 cases of enterococcal bacteremia which occurred from 1988 to 1992. Twenty-seven cases had no medical charts, dismissing possibility of evaluation. Finally, 181 cases of enterococcal bacteremia were analysed. RESULTS: One hundred and eighteen episodes were nosocomial infections. Polymicrobial bacteremia occurred in 68.5% of the patients and the most common co-isolate was Pseudomonas aeruginosa. Those patients (78.5%) with underlying diseases and malignancies were the most common underlying problems. The portal of entry could be found in 69.6 percent of patients, with the gastrointestinal tract the most common sources. Antimicrobial susceptibility testing showed high gentamicin resistance rate (89.5%), and ampicillin still had about 80 percent sensitivity rate. The group who received specific antibiotic therapy for enterococcus showed lower mortality (36.4% versus 47.6%). Only one case had infective endocarditis. Forty-nine patients suffered from septic shock, the cause of 30 deaths. Totally 75 patients died during hospitalization. Besides sepsis, another major cause of death was their underlying diseases itself. CONCLUSIONS: Enterococci have no doubt become important nosocomial pathogens and enterococcal bacteremia were associated with high mortality, especially in elderly patients with underlying diseases such as malignancy or diabetes. When clinically dealing with sepsis from the gastrointestinal or biliary tract, especially when previous cephalosporins therapy showed no response, the possibility of enterococcal bacteremia should always be considered.     

Intralesional radiolabeled human monoclonal IgM in human tumor xenografts

Sensory-perceptual abnormalities in people with autism are discussed from two perspectives: published firsthand accounts and existing psychological research evidence. A range of abnormalities, including hyper- and hyposensitivity, sensory distortion and overload, and multichannel receptivity and processing difficulties, are described in firsthand accounts and frequently portrayed as central to the autistic experience. A number of dangers are inherent in uncritically accepting these accounts at face value and in any wider generalization to the autistic population as a whole. Evidence from clinical studies suggests that unusual sensory responses are present in a majority of autistic children, that they are manifested very early in development, and that they may be linked with other aspects of autistic behavior. In addition, experimental studies using a range of indices have found evidence of unusual responses to sensory stimuli in autistic subjects. However the clinical and experimental research to date suffers from serious methodological limitations and more systematic investigation is warranted. Key issues for future psychological research in the area are identified.     

Problems in the hygienic rationalization of the therapeutic and prophylactic nutrition of industrial workers

Based on generalization and analysis of instructions and guidelines for therapeutical and prophylactic diets of workers, ways of its optimization were proposed, by using bifide-containing acid dairy products as a preventive agent against possible occupational diseases caused by occupational factors.     

Control of locomotion in the marine mollusc Clione limacina. XI. Effects of serotonin

The locomotor activity in the marine mollusc Clione limacina has been found to be strongly excited by serotonergic mechanisms. In the present study putative serotonergic cerebropedal neurons were recorded simultaneously with pedal locomotor motoneurons and interneurons. Stimulation of serotonergic neurons produced acceleration of the locomotor rhythm and strengthening of motoneuron discharges. These effects were accompanied by depolarization of motoneurons, while depolarization of the generator interneurons was considerably lower (if it occurred at all). Effects of serotonin application on isolated locomotor and non-locomotor pedal neurons were studied. Serotonin (5 x 10(-7) to 1 x 10(-6) M) affected most pedal neurons. All locomotor neurons were excited by serotonin. This suggests that serotonergic command neurons exert direct influence on locomotor neurons. Effects of serotonin on nonlocomotor neurons were diverse, most neurons being inhibited by serotonin. Some effects of serotonin on locomotor neurons could not be reproduced by neuron depolarization. This suggests that, along with depolarization, serotonin modulates voltage-sensitive membrane properties of the neurons. As a result, serotonin promotes the endogenous rhythmical activity in neurons of the C. limacina locomotor central pattern generator.     

Prognostic significance of cathepsin-D in patients with breast cancer

The expression of the protease cathepsin-D has been evaluated using an immunohistochemical technique with a polyclonal antibody in paraffin-embedded tissue from 359 patients treated between the years 1975-1981 for Stage I and II breast cancer. One hundred and twenty seven patients (35%) have strongly positive, granular staining, 138 (38%) are intermediately stained in the cytoplasm, and in 94 (26%) no staining is observed. There is a strong positive association between expression of cathepsin-D and the presence of tumour in axillary lymph nodes (P < 0.006). Expression of the protease is associated with significantly poorer survival of patients in univariate analysis (P = 0.025); however, this is not independent of other tumour variables.     

Gene amplification in a p53-deficient cell line requires cell cycle progression under conditions that generate DNA breakage

Amplification of genes involved in signal transduction and cell cycle control occurs in a significant fraction of human cancers. Loss of p53 function has been proposed to enable cells with gene amplification to arise spontaneously during growth in vitro. However, this conclusion derives from studies employing the UMP synthesis inhibitor N-phosphonacetyl-L-aspartate (PALA), which, in addition to selecting for cells containing extra copies of the CAD locus, enables p53-deficient cells to enter S phase and acquire the DNA breaks that initiate the amplification process. Thus, it has not been possible to determine if gene amplification occurs spontaneously or results from the inductive effects of the selective agent. The studies reported here assess whether p53 deficiency leads to spontaneous genetic instability by comparing cell cycle responses and amplification frequencies of the human fibrosarcoma cell line HT1080 when treated with PALA or with methotrexate, an antifolate that, under the conditions used, should not generate DNA breaks. p53-deficient HT1080 cells generated PALA-resistant variants containing amplified CAD genes at a frequency of >10(-5). By contrast, methotrexate selection did not result in resistant cells at a detectable frequency (<10(-9)). However, growth of HT1080 cells under conditions that induced DNA breakage prior to selection generated methotrexate-resistant clones containing amplified dihydrofolate reductase sequences at a high frequency. These data demonstrate that, under standard growth conditions, p53 loss is not sufficient to enable cells to produce the DNA breaks that initiate amplification. We propose that p53-deficient cells must proceed through S phase under conditions that induce DNA breakage for genetic instability to occur.     

Book review: Media violence and its effects on aggression: Assessing the scientific evidence.

Review of book: Media violence and its effects on aggression: Assessing the scientific evidence, by Jonathan L. Freedman. Toronto: ON: University of Toronto Press, 2002, 227 pp. Hardcover. ISBN 0-8020-3553-1. Reviewed by Claire Crooks. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of benfluorex metabolites on membrane fluidity and insulin-related processes

Hepatocyte growth factor (HGF) is a potent mitogen for the maturation of hepatocytes in vitro which plays a role in liver regeneration in vivo. In addition, transforming growth factor-beta 1 (TGF-beta 1) is also a potent regulator of liver regeneration. In attempting to clarify the mechanisms related to liver regeneration after partial hepatectomy, we investigated the expression of HGF and TGF-beta 1 in rats with liver cirrhosis (LC). A rat model of LC was prepared using carbon tetrachloride (CCl4). The expression of HGF mRNA in both the LC and control groups showed a similar time-course with the highest expression seen at 18h after a 70% hepatectomy. The expression of TGF-beta 1 mRNA peaked at 18h after partial hepatectomy in the LC group and at 48h in the control group. The 5-bromo-2'-deoxyuridine (BrdU) labeling index for the LC group at 24, 48, and 72 h after partial hepatectomy was 9.2%, 5.9%, and 1.8%, while for the control group it was 7.0%, 11.7%, and 6.8%, respectively. The BrdU labeling index in the LC group was thus suppressed earlier than that in the control group. We therefore postulate that regeneration of the remnant liver in the presence of LC accelerates immediately after partial hepatectomy, but the extent of regeneration is insufficient because of an early cessation due to an early expression of TGF-beta 1.